IRTKS negatively regulates antiviral immunity through PCBP2 sumoylation-mediated MAVS degradation

Pengyan Xia, Shuo Wang, Zhen Xiong, Buqing Ye, Li-Yu Huang, Ze-Guang Han () and Zusen Fan ()
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Pengyan Xia: Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences
Shuo Wang: Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences
Zhen Xiong: Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences
Buqing Ye: Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences
Li-Yu Huang: Key Laboratory of Systems Biomedicine (Ministry of Education) and Collaborative Innovation Center of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University
Ze-Guang Han: Key Laboratory of Systems Biomedicine (Ministry of Education) and Collaborative Innovation Center of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University
Zusen Fan: Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract RNA virus infection is recognized by the RIG-I family of receptors that activate the mitochondrial adaptor MAVS, leading to the clearance of viruses. Antiviral signalling activation requires strict modulation to avoid damage to the host from exacerbated inflammation. Insulin receptor tyrosine kinase substrate (IRTKS) participates in actin bundling and insulin signalling and its deficiency causes insulin resistance. However, whether IRTKS is involved in the regulation of innate immunity remains elusive. Here we show that IRTKS deficiency causes enhanced innate immune responses against RNA viruses. IRTKS-mediated suppression of antiviral responses depends on the RIG-I-MAVS signalling pathway. IRTKS recruits the E2 ligase Ubc9 to sumoylate PCBP2 in the nucleus, which causes its cytoplasmic translocation during viral infection. The sumoylated PCBP2 associates with MAVS to initiate its degradation, leading to downregulation of antiviral responses. Thus, IRTKS functions as a negative modulator of excessive inflammation.

Date: 2015
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DOI: 10.1038/ncomms9132

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